Page 990 - Small Animal Clinical Nutrition 5th Edition

Gastritis/Gastroduodenal Ulcers 1027

gastritis including the basenji, Norwegian lundenhund and Table 52-1. Potential causes of gastritis and/or
VetBooks.ir Drentse patrijshond (Slappendel et al, 1997; Hart, 2004; Simp- gastroduodenal ulceration.
son, 2005, 2006; Berghoff et al, 2007). Racing sled dogs in
Adverse reactions to food
competition are at increased risk for gastroduodenal erosions
and ulceration although dogs in training are not (Davis et al, Food allergy (hypersensitivity)
Food intolerance
2006). Nearly 50% of dogs completing the Iditarod race were Dietary indiscretion
found to have gastric lesions (Davis et al, 2003, 2003a). Chemicals
Foreign bodies
Garbage toxicosis
Etiopathogenesis Gluttony
Acute Gastritis and Gastroduodenal Ulceration Heavy metal toxicosis
Acute gastritis is characterized by sudden-onset vomiting, Plants
Drug administration
resulting from gastric mucosal insult or inflammation. Corticosteroids
Hematemesis usually indicates that gastroduodenal erosions Nonsteroidal antiinflammatory agents
or ulcerations are present (Willard, 2005). Gastroduodenal Idiopathic gastritis
Infectious agents
ulceration occurs following disruption of the gastric mucosal Fungi
barrier. The gastric mucosal barrier is a group of physical and Parasites
chemical defense mechanisms designed to protect the gastric Spiral bacteria
Inflammatory bowel disease
mucosa from insults leading to erosions or ulcers. Disruption Neoplasia
of the gastric mucosal barrier may involve direct injury, Gastrinoma
decreased mucosal blood flow, alterations in protective Mastocytosis
Primary gastric neoplasia
prostaglandins (prostaglandin E [PGE ]) or hypersecretion Reduced gastric blood flow
2
2
of gastric acid (e.g., gastrinoma) (Simpson, 2005; Henderson Disseminated intravascular coagulopathy
and Webster, 2006). Neurologic disorders
Sepsis
Several metabolic disorders are associated with acute gastri- Shock
tis and gastroduodenal ulceration (Table 52-1). Uremia may Reflux gastritis
result in diffuse GI tract hemorrhage. GI erosions and ulcers Systemic disease
Hypoadrenocorticism
are thought to result from effects of uremic toxins on the gut Kidney disease
mucosa. Additionally, increased circulating concentrations of Liver disease
gastrin have been identified in patients with uremia. The kid- Pancreatitis
neys normally excrete up to 40% of circulating gastrin.
Clearance of gastrin is decreased with chronic kidney disease.
The resulting hypergastrinemia leads to increased acid produc- genesis of mucosal ulceration associated with hepatopathies is
tion. Studies suggest that hypersecretion of gastrin may con- multifactorial and associated coagulopathies may worsen clini-
tribute to gastric ulceration in chronic kidney disease cal manifestations.Potential mechanisms include altered gastric
(Thornhill, 1983; Peters et al, 2005; Polzin et al, 2005; blood flow due to portal hypertension, delayed epithelial turn-
Henderson and Webster, 2006). over, gastric hyperacidity and hypergastrinemia. Experimental
GI signs and histopathologic changes are seen in dogs with evidence suggests that hypergastrinemia is a less important
chronic kidney disease. A retrospective study was done to mechanism than previously suspected (Booth, 1990; Hen-
determine the prevalence of gastric histopathology in necropsy derson and Webster, 2006).
samples from 28 dogs with chronic kidney disease and to char- A variety of adverse drug reactions have been reported fol-
acterize the histopathologic changes. All dogs presented with lowing the use of NSAIDs in dogs.These include GI bleeding,
GI signs, including anorexia and vomiting. Twenty-two (79%) ulceration or both and hepatotoxicity and nephrotoxicity (Sen-
of the 28 dogs had gastric pathology. The most common nello and Leib, 2006). The adverse GI effects occur because
pathology included edema, vasculopathy, glandular atrophy and some NSAIDs have a topical irritant effect on the gastric
mineralization. No evidence of ulceration was seen histopatho- mucosa and can inhibit protective prostaglandins (McCarthy,
logically and only one dog had ulceration noted on gross 1999; Enberg et al, 2006). Experimentally induced and sponta-
necropsy. Dogs with higher serum biochemistry scores (i.e., neous gastritis and gastroduodenal ulcerations have been
blood urea nitrogen, creatinine and calcium-phosphorus prod- reported to occur in dogs in conjunction with the use of
uct) were more likely to have gastric pathology. The authors NSAIDs, including aspirin, indomethacin, naproxen, ibupro-
concluded that gastric ulceration may be uncommon in dogs fen, phenylbutazone, flunixin meglumine, piroxicam, sulindac
with chronic kidney disease (Peters et al, 2005). and meclofenamic acid (Dow et al, 1990; Lipowitz et al, 1986;
Liver disease is a common cause of GI ulcerations, which Wallace et al, 1990; Davenport, 1992). The ulcerogenicity of
may be manifested as hematemesis.Liver disease was one of the NSAIDs is attributed to inhibition of the enzyme cyclooxyge-
two most common risk factors (the other being treatment with nase (COX) in the prostaglandin synthesis pathway,resulting in
NSAIDs) in a retrospective study of 43 dogs with gastroduo- the loss of the gastric protective effects of prostacyclin and
denal ulceration (Henderson and Webster, 2006). The patho- prostaglandin E (Davenport, 1992).